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Background  The Phosphatidylinositol 3′-kinase is a key regulator in various cancer-associated signal transduction pathways. Genetic alterations of its catalytic subunit alpha,  PIK3CA , have been identified in ovarian cancer. Our  in vivo  data suggests that  PIK3CA  activation is one of the early genetic events in ovarian cancer. However, its role in malignant transformation of ovarian surface epithelium (OSE) is largely unclear.    Methodology/Principal Findings  Using the Müllerian inhibiting substance type II receptor (MISIIR) promoter, we generated transgenic mice that expressed activated  PIK3CA  in the Müllerian epithelium. Overexpression of  PIK3CA  in OSE induced remarkable hyperplasia, but was not able to malignantly transform OSE  in vivo . The consistent result was also observed in primary cultured OSEs. Although enforced expression of  PIK3CA  could not induce OSE anchorage-independent growth, it significantly increased anchorage-independent growth of OSE transformed by mutant  K-ras .    Conclusions/Significance  While  PIK3CA  activation may not be able to initiate OSE transformation, we conclude that activation of  PIK3CA  may be an important molecular event contributing to the maintenance of OSE transformation initiated by oncogenes such as  K-ras .

Expression of Activated PIK3CA in Ovarian Surface Epithelium Results in Hyperplasia but Not Tumor Formation